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The mutation 501Y, which is present in both lineages from the UK (501Y.V1) and SA (501Y.V2) shows an increased affinity to the entry receptor Ace2. This was mainly known already. It is fair to assume that the ~50% higher transmission rate is associated with this increase
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1/n
binding to Ace2.
Now was a new mutation seen in Brazil that contains a double mutation 484K and 501Y in the same virus.
Coincidentally, I was just able to be part of a study (lead by the Schreiber lab) that found exactly this double mutant in experimental evolution studies
2/n
Now was a new mutation seen in Brazil that contains a double mutation 484K and 501Y in the same virus.
Coincidentally, I was just able to be part of a study (lead by the Schreiber lab) that found exactly this double mutant in experimental evolution studies
2/n
While the single 501Y mutations causes a ~2.5x higher affinity to Ace2, the double mutation results in a ~13x higher affinity to Ace2 compared to the WT version. https://www.biorxiv.org/content/10.1101/2021.01.06.425392v1.full.pdf
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3/n
I'm not saying that this new double mutation with the much higher affinity to Ace2 is even more transmissible - viruses are much more complex than this and often, with other viruses, we have seen that tighter binding is actually bad for the virus. If this was the case,
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4/n
The virus would require further compensatory mutations that alter this "too tight" binding and "loosens" this a little again - guess we will see
However, bottomline for me (at least for now) until we know more about the Brazialian variant, it is most certainly of big interest
5/5
However, bottomline for me (at least for now) until we know more about the Brazialian variant, it is most certainly of big interest
5/5
Ps, I should add this here so more read it: as pointed out both, the SA & BR variants, have the double mutation. While the SA variant also, carries a 2 amino acid deletion, the BR variant does not. Both also have other mutations. None of which we know the function of (if any)yet
